Acute Heart fail Drugs (pt 2 HF cases)

Question 1

Dopamine actions

Answer 1

Stimulates release of catecholamines

Always hypothesized to be renal protective, but has never been shown to clinically significant.

Question 2

Dosing of Dopamine changes it’s affects at
low doese of 2-5 mcg/kg/min:
doses greater then 6 mcg/kg/min:
doses of 10 mcg/kg/min:

Answer 2

Lower doses 2-5 mcg/kg/min exert effects on dopamine receptors and b receptors.
At doses greater than 6 mcg/kg/min:tachycardia without increased inotropypredominates.
at 10 mcg/kg/min: Afterload increases due to effects on a receptors

Question 3

ACtion of Dobutamine:

Answer 3

Predominant action is a β1 agonist with weak β2 activity.

Increases contractility with mild vasodilator effect.

Question 4

Predominant action is a β1 agonist with weak β2 activity.

Increases contractility with mild vasodilator effect.

Answer 4

Dobutamine

Question 5

Side effect of Dobutamine

Answer 5

1. ARRHYTHMIA
2. ANGINA
3. HYPERTENSION
4. TACHYCARDIA

Question 6

Levosimendan

Answer 6

Calcium sensitizer and Vasodilator
Acts on Troponin C to increase its sensitivity to calcium.
At high concentrations can be a phosphodiesterase III inhibitor

Question 7

Acts on Troponin C to increase its sensitivity to calcium.

At high concentrations can be a phosphodiesterase III inhibitor

Answer 7

Levosimednan

Question 8

Levosimendan effects on:
LVEDP:
Afterload:
SV:

Answer 8

Decrease LVEDP
Decrease Afterload
Increase Stroke Volume

Question 9

What are the issues when using ionotropes in ADHF?

Answer 9

Arrythmias, hypotension, increased troponin release, increases in-hospital stay and 6 month mortality, doesn’t decrease hospital stay

Question 10

What do we have to keep in mind when dosing diuretics in Heart fail pts?

Answer 10

dosing needs to be higher to achieve same effect we seen in non-HF pts.

Question 11

What is the Braking phenomenon in regards to diuretic therapy?

Answer 11

“Braking” phenomenon
– Long-term loop diuretic administration results in a reduced natriuretic response
– Relative or absolute contraction of the extracellular fluid volume,
resulting in reduced delivery of solute to the proximal tubule via the RAAS and SNS as well as by enhanced distal nephron solute
reabsorption via adaptive epithelial hypertrophy and hyper function.

Question 12

What is “rebound” phenomenon in regards to diuretics?

Answer 12

“Rebound”
– Infrequent dosing may lead to sodium retention that exceeds natriuresis.
– Divided doses to help with this, but hold off on it as long as possible

Question 13

Why is long term tolerance an issue in Diuretic therapy in HF pts?

Answer 13

Long-term Tolerance

– Tubular hypertrophy to compensate for salt loss

Question 14

Pt comes in with heart fail and your attending stays you will start them on diuretics, which one do you start them on?

Answer 14

Furosemide admin first; in IV as bolus or continous… if it’s refractory… switch to bumetadine

Question 15

What type of electrolyte abnormalities do we see in diuretics?

Answer 15

 HYPOKALEMIA
 HYPOMAGNESEMIA
 HYPONATREMIA

Question 16

These drugs cause renal insufficiency when given with digoxin as well as gout exacerbation and cause muscle cramps if given too quickly.

Answer 16

Diuretics

Question 17

You attending had you administered Bumetanide adn mirinone to pt in heart fail. Their saturation went up to 68% but the congestion isn’t improving… what do you do next?

Answer 17

re-eval (most likely have Na and fluid restriction)
Increase doses of loop diuretic or do continuous infusion. Additionally, add a second type of diuretic orally (metolazone or spironolactone)or IV chlorothaized

Question 18

74 yo w/ longstanding history of poorly controlled HTN, DM and dyslipidemia; presents saturday AM with shortness of breath and wt gain; went to fish fry, didn’t take meds and took ibuprofen for back pain: medications include atenolol 25mg twice daily, HCTZ 25mg
daily, atorvastatin 20mg daily
BP 178/94 mm Hg, HR 90
• PE: Regular, crisp S1, S2, +S3, +S4
• JVP 8cm above clavicle
• Lungs clear with decreased BS at both bases
• 2+ LE edema
• Labs: Normal, except for NT-pro-BNP 4000
Dx?

Answer 18

Warm and Wet
increased JVD is sign of ‘wet’ as well as the LE edema (or any edema)
Not seeing signs of renal dysfunction or note of cool extremeties and labs aren’t showing renal dysnfunction so we think more warm as all those listed are signs of cool

Question 19

Most pts wth acute decompensated HF fall into what category?

Answer 19

Wet and Warm

Question 20

What are our key therapy goals in pts with wet and warm heart fail?

Answer 20

Decrease the filling pressures (LVEDP and PCWP)

Most of the time use IV diuretics and may need vasodialators

Question 21

What vasodialators do we use in ADHF?

Answer 21

Nitroglycerin, nitroprusside, nesiritide

Question 22

Effects of increasing doses of vasodialators:
Afterload:
Stroke Volume:
LVEDP:
Preload:

Answer 22

Afterload decreases
SV increases
LVEDP decreases
Preload decreases

Question 23

IV nitroglycerin hemodynamic effects:

Answer 23

venodialator; arterial vasodilator at high doses
decreases filling pressure at low doses; at high doses, decreases SVR and increases cardiac output
Increased coronary blood flow

Question 24

IV nitroglycerin has several major limitations; what are they?

Answer 24

headache, hypotension (especially if filling pressures are low), prolounged profound hypotension and bradycardia (rare), tachyphylaxsis and 20% don’t respond

Question 25

Nitropusside hemodynamic effects

Answer 25

Balanced vasodilator for both veins and arterioles and decreases filling pressure, SVR, PVR, and increases CI

Question 26

venodialator; arterial vasodilator at high doses
decreases filling pressure at low doses; at high doses, decreases SVR and increases cardiac output
Increased coronary blood flow

Answer 26

IV introglycerin

Question 27

Major limitations of nitroprusside:

Answer 27

Cyanide toxicity; manifested by nausea and ‘feeling weird’ and seen with higher doses
occurs in setting of low hepatic reperfusion d/t low CO
Accumulation of thiocynate: occur over days during chronic use; especially with impaired renal function

Question 28

Pt has Wet and Warm heart fail, what drugs in additoin to diuretics should we give them?

Answer 28

NONE:
ionotropes; ischemia/arrythmias and death
nesiritide: placebo
vasopressin antagonist: no sustained benefit

Question 29

You are trying to decide if you should give IV vasodialtors or ionotropes to pt with heart fail… how do you make your decission?

Answer 29

depends on systemic vascular resistance and BP
If SVR is high, check the SBP!
SBP >/= 85mmHg: use Vasodialtor
SBP< 85mmHg: use Ionotrope + IABP

Question 30

Pt has SBP of 100mmHg, do you use vasodialator or ionotrope +IABP?

Answer 30

over 85mmHg use Vasodialator; if its under use ionotrope

Question 31

When do you give pt nitroprusside if they have acute decompensated heart fail? and does it help overall mortality?

Answer 31

for pts with SBP above 85mmHg and it does help with mortality

Question 32

Mech of ACE inhibitors targeting afterload:

Answer 32

Inhibition of Angiotensin binding of the AT1
receptor to stimulate vasoconstriction
AT1: vasoconstriction, cell growth/prolif/ aldosterone release/ Na and water retention/ CV hypertrophy/ inhibits renin release

Question 33

What does AT2 do?

Answer 33

vasoD, inhibits hypertrophy, antiproliferation, antiproliferation, mediates NO and PGI2, renal Na excreation

Question 34

Not currently approved in the United States. It is sensitizes myofilaments to calcium,
and opens peripheral potassium channels in the vasculature.

Answer 34

Levosimendan:

Question 35

Mixed alpha and beta agonist depending on the dose used.
1-5 mcg/kg/min stimulates
contractility.
Increasing dose > 5mcg/kg/min stimulates heart rate and vasoconstriction.

Answer 35

Dopamine

Question 36

Phosphodiesterase 3 inhibitor acts by preventing the degradation of cAMP thereby
increasing the amount of bioavailable cAMP. Severe hypotension if bolused

Answer 36

milrinone

Question 37

Beta agonist increases heart rate and contractility, but also peripheral vasodilation.

Answer 37

Dobutamine

Question 38

drugs work on increasing myocardial contractility through stimulation of the beta adrenergic
receptor, or through intracellular signaling which results in changes in intracellular calcium

Answer 38

Ionotropes

Question 39

Major issue with ionotropes and what type of heart fail pt gets them?

Answer 39

major complications of all these medications are the increased risk of tachyarrythmias, and most also
cause hypotension. They are reserved for the cold and wet patient who is refractory to other therapies

Question 40

Why is the use of vasodialtors so important at an afterload reducer?

Answer 40

ejection period starts when aortic valve opens, if pressure of aorta can be decreased, the aorta will open earlier and allow more blood to eject per Stroke… ultimately reduces BP